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Vol. 83, Issue 5, 1630-1634, 1997
1 Laboratory for Exercise and Environmental Medicine, at the Health, Leisure, and Human Performance Research Institute, and Department of Anesthesia, Faculty of Medicine, University of Manitoba, Manitoba R3T 2N2; and 2 Department of Biology, University of Victoria, Victoria, British Columbia, Canada V8W 2Y2
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Giesbrecht, Gordon G., M. S. L. Goheen, C. E. Johnston, G. P. Kenny, Gerald K. Bristow, and John S. Hayward. Inhibition of
shivering increases core temperature afterdrop and attenuates rewarming
in hypothermic humans. J. Appl.
Physiol. 83(5): 1630-1634, 1997.
During severe
hypothermia, shivering is absent. To simulate severe hypothermia,
shivering in eight mildly hypothermic subjects was inhibited with
meperidine (1.5 mg/kg). Subjects were cooled twice (meperidine and
control trials) in 8°C water to a core temperature of 35.9 ± 0.5 (SD) °C, dried, and then placed in sleeping bags. Meperidine
caused a 3.2-fold increase in core temperature afterdrop (1.1 ± 0.6 vs. 0.4 ± 0.2°C), a 4.3-fold increase in afterdrop duration
(89.4 ± 31.4 vs. 20.9 ± 5.7 min), and a 37% decrease in
rewarming rate (1.2 ± 0.5 vs. 1.9 ± 0.9°C/h).
Meperidine inhibited overt shivering. Oxygen consumption, minute
ventilation, and heart rate decreased after meperidine injection but
subsequently returned toward preinjection values after 45 min
postimmersion. This was likely due to the increased thermoregulatory
drive with the greater afterdrop and the short half-life of
meperidine. These results demonstrate the effectiveness of shivering
heat production in attenuating the postcooling afterdrop of core
temperature and potentiating core rewarming. The meperidine protocol
may be valuable for comparing the efficacy of various hypothermia
rewarming methods in the absence of shivering.
first aid; rate of rewarming; shivering thermogenesis; hypothermia
treatment
INTRODUCTION IT IS GENERALLY AGREED that treatment of the
hypothermic victim should minimize the postexposure afterdrop in core
temperature (Tco) and promote a
steady continuous rate of rewarming to a level at which thermal,
cardiorespiratory, and metabolic homeostasis can be maintained. The
appropriate method of treatment may depend on the level of hypothermia.
In mild-to-moderate hypothermia, vigorous shivering produces
considerable endogenous heat, which often masks potential benefits of
various exogenous rewarming techniques (5, 13, 15, 16). One notable
sign of severe hypothermia is the termination of shivering (12). The
consequent decrease in endogenous heat production would likely result
in a greater postcooling fall in
Tco (afterdrop) and minimize any potential for spontaneous core rewarming. Such a condition would be
unfavorable because the terminal event in accidental hypothermia is
usually cold-induced ventricular fibrillation or cardiac arrest (2).
Therefore, the magnitude of the effect of shivering suppression would
be a valuable factor when consideration is given to treatment strategies for severe hypothermia.
In-depth study of severe hypothermia is difficult because experimental
study of humans is confined to mild hypothermia
(Tco > 33-35°C),
whereas clinical reports are generally retrospective and involve highly
variable circumstances. To evaluate the possible importance of
shivering suppression, we have developed a human protocol that inhibits
shivering, decreases metabolism, and produces cold body tissue, with
appropriate periphery-to-core temperature gradients, within clinically
safe Tco limits. The
narcotic drug meperidine is commonly used to inhibit postoperative
shivering (22). Because it has immediate onset when given intravenously and has a short duration of action (2-4 h) (20), this drug is attractive for experimental use to effectively abolish shivering during
mild hypothermia.
To evaluate the possible importance of shivering suppression associated
with severe hypothermia, we induced immersion hypothermia in human
volunteers and compared physiological responses during two spontaneous
rewarming protocols: 1) with
shivering intact and 2) with
shivering inhibited by meperidine. We hypothesized that the inhibition
of shivering heat production would result in a greater postimmersion
afterdrop in Tco with little or no subsequent increase in Tco.
METHODS
O2) was
determined by an open-circuit method from measurements of expired
minute ventilation (E) and inspired and
mixed expired gas concentrations sampled from a 10-liter fluted mixing
box. E was monitored by a
pneumotachometer (model 47304A flow transducer, Hewlett-Packard) placed
in the expiratory circuit proximal to the mixing box. Mixed expired
oxygen was sampled from the mixing box at 500 ml/min and analyzed by a
Beckman OM-11 O2 sensor (Beckman,
Anaheim, CA) for O2 fraction.
Analog data from the thermocouples, thermal flux transducers, gas
analyzer, and pneumotachometer were acquired by using an electrically
isolated Macintosh IIci computer. Data were scaled by using appropriate
corrections and, where applicable, the calculated BSA. At 30-s
intervals, the results were averaged for the preceding 30-s period,
displayed graphically on the computer screen, and recorded in
spreadsheet format on a hard disk. The process was controlled by a
"virtual instrument" written by using LabVIEW II graphic
signal-processing software (National Instruments, Austin, TX).
Protocol.
Before immersion, subjects sat quietly for a period of 10 min, during
which baseline data were collected. For both trials, they were then
immersed (by using an electrically isolated hoist) to the sternal notch
in a stirred water bath in which the water temperature was lowered from
20 to 8°C within 10 min by the addition of ice. They remained in
the water until the final injection was made (see below). An attempt
was made to adjust immersion time such that drug or placebo injections
would be complete, and the subjects removed from the cold water, at a
Tes of 36°C. This required between 35 and 70 min, depending on individual body composition and
metabolic response to cooling. Greater core cooling was not attempted
because this length of cold-water immersion was sufficient to produce
significant tissue cooling, and further increases in thermal stimuli
may necessitate higher doses of meperidine for complete suppression of
shivering. For comparative purposes, the immersion time and removal
Tes for each subject were kept
similar for both control and meperidine trials.
Intravenous injections began 10 min before cold water exit. In the
meperidine trial, 1.5 mg/kg of meperidine (diluted in 10 ml of saline)
were injected in five equal boluses at 2-min intervals before the
subjects exited the water. In the control trial, equal volumes of
saline were injected. After the injection period, subjects were hoisted
from the tank directly onto a bed where they were seated and quickly
towel dried. They then lay down inside a sleeping bag for between 30 and 145 min. In each trial, enough data were collected to establish a
clear linear rate of rewarming. Subjects then were immersed in warm
(38°C) water for ~25 min to complete rewarming. The order of the
trials followed a balanced design.
Data analysis.
All data were averaged for the baseline period (10 min) and for
subsequent 5-min intervals during immersion and postimmersion. The
following rewarming variables were calculated for each trial: the
afterdrop (difference between Tes
on exit from cold water and its nadir), length of the afterdrop period
(time between exit from cold water until
Tes returned to original exit
Tes), and the rate of rewarming
(calculated by linear regression for
Tes data during the linear
increase after the Tes nadir).
O2 was converted to heat
production by assuming a constant mixed respiratory exchange ratio of
0.83 and setting 1 l O2/min
equivalent to 340.4 W (9). Heat production values greater than baseline
were attributed to shivering. Total cutaneous heat flux and mean
Tsk were calculated. Net heat gain
was then calculated by subtracting total cutaneous heat flux (positive
values indicate heat loss to the environment) from metabolic heat
production. Respiratory heat loss was considered minimal and therefore
not included in these calculations. For each time interval, the rate of
net heat gain was converted from watts to kilocalories per minute (1 W = 0.014 kcal/min). The cumulative change in body heat content was then
calculated. Data for the two trials were compared by using paired
t-tests. Results are reported as means ± SD. P < 0.05 identified
statistically significant differences.
RESULTS
Subjects were closely monitored for adverse affects during the serial meperidine injections. On completion of the final injection, each subject reported relief from cold discomfort, and visible shivering was abolished. Although the subjects were conscious under these conditions, their mental responses were obtunded.
Tco responses. During immersion, Tes decreased at a similar rate for both conditions (Fig. 1). Tes was significantly lower with meperidine from 10 min postimmersion to the end of the rewarming period (P < 0.01). The afterdrop with meperidine (1.1 ± 0.6°C) was three times greater than during control (0.4 ± 0.2°C; P < 0.005). Similarly, the afterdrop length was over four times longer during meperidine (89.4 ± 31.4 min) than during control (20.9 ± 5.7 min) trials (P < 0.0001). The rewarming rate during control (1.9 ± 0.9°C/h) was significantly higher than with meperidine (1.2 ± 0.5°C/h; P < 0.05).
Metabolic and cardiorespiratory responses. Before injections, shivering heat production increased throughout cooling (Fig. 1). In the control trials,
O2 continued to increase,
with maximum values coinciding with the nadir in Tes. Meperidine injection caused a
rapid decrease in shivering, with
O2 falling continually until
15 min postimmersion. O2 then
rose gradually over the next 30 min, indicating diminished inhibition
by meperidine of shivering heat production. This partial recovery of
shivering was associated with termination of the relatively large
afterdrop and subsequent slow rewarming rate.
E paralleled the
O2 results for both
treatments, rising steadily from 11.1 ± 2.3 l/min during baseline
to 18.9 ± 6.4 l/min just before injections. In the control trials,
E continued to increase to a maximum
value of 26.4 ± 6.4 l/min 15 min postimmersion and subsequently
decreased to baseline values over the next 45 min.
E for meperidine trials was significantly
lower than for control for the final 5 min of immersion and throughout
the postimmersion period (P < 0.005). After meperidine injections, E
steadily decreased to below baseline levels by 15 min postimmersion.
E then rose to 13.1 ± 2.0 l/min 45 min postimmersion and subsequently decreased toward baseline.
Heart rate was similar in the two conditions during baseline and
cooling periods before the start of injections, with rates remaining
near baseline values (Fig. 2). During
control, heart rate then rose slightly until 10 min postimmersion
followed by a decrease to subbaseline values. In the meperidine trial,
heart rate decreased after meperidine injection until 10 min
postimmersion and remained below baseline values for the remainder of
the postimmersion period. During the meperidine trials an abrupt rise
of short duration immediately postimmersion coincided with the transfer
period and may reflect cardiac excitation above the
meperidine-inhibited level due to voluntary motor activity
and/or postural changes.
Heat transfer. Cutaneous heat flux increased similarly in control and meperidine trials, from 103 ± 15 W during baseline to 465 ± 129 W early in immersion with a subsequent decrease to 382 ± 91 W by the end of immersion. Postimmersion heat flux stabilized at a higher value during control trials (61 ± 20 W) than during meperidine trials (43 ± 12 W) (P < 0.05). Net heat gain was similar in both conditions until injections (Fig. 3). Postimmersion net heat gain was consistently greater in the control trials by 87-158 W with the differences being significant for the first 15 min (P < 0.05). During cooling the cumulative change in body heat content was similar in both conditions (Fig. 3). Postcooling body heat content was restored at a greater rate during control trials.
In both conditions, mean Tsk decreased from baseline values of 32.6 ± 0.6 to 21.7 ± 1.8°C throughout the immersion period. During postimmersion in the control trials, Tsk increased continually to a value of 30.5 ± 1.3°C after 30 min. In the meperidine trials, mean Tsk increased at a slower rate, to only 29.0 ± 1.6°C after 30 min postimmersion and finally reaching 31.8 ± 1.3°C after 80 min. Mean Tsk was significantly greater in control vs. meperidine trials from 15 min postimmersion until the end of the trials (P < 0.02).
DISCUSSION
Meperidine effectively blocked shivering heat production for sufficient time to clearly demonstrate the effectiveness of shivering in minimizing the magnitude of postcold exposure afterdrop of Tco. Inhibition of shivering in the meperidine trials resulted in a threefold increase in Tco afterdrop and more than a fourfold increase in length of the afterdrop period. Although Tco did increase late in the meperidine trials, the rewarming occurred at a very low rate and did not commence until ~30 min after the slight disinhibition of shivering occurred.
Afterdrop values for the control condition (0.4°C) were within the range previously reported for shivering subjects (0.0-0.6°C) (3, 5, 10, 11, 13, 19). In the meperidine condition the afterdrop (1.1°C) was greater than previously reported in subjects who were not actively warmed (3, 5, 10, 11, 13, 19). Collis et al. (5) cooled nine subjects in 7.5°C water to Tco of 35°C and reported that three of the subjects did not shiver overtly during rewarming. The increase in tympanic temperature afterdrop in their spontaneously nonshivering subjects (0.80°C), compared with their shivering subjects (0.55°C), was qualitatively similar to our present results, although their nonshivering-to-shivering afterdrop ratio (1.5) was less than we report (3.2).
The rate of rewarming for the control shivering-intact condition
(1.9°C/h) was within the range of rewarming rates previously reported for shivering subjects (0.6-4.9°C/h) (3, 5, 10, 11,
13, 19, 23, 26). The rate during nonshivering meperidine trials
(1.2°C/h) was near the minimum values previously reported for human
subjects (23, 26). Although Collis et al. (5) studied three apparently
nonshivering subjects, they did not measure O2 or report individual
rewarming rates; therefore, a comparison of our nonshivering data with
other nonshivering subjects is not possible.
The magnitude of Tco afterdrop depends on the following factors: conductive heat loss along tissue thermal gradients (18, 27), convective heat loss through changes in peripheral blood flow (4, 10), and local metabolic heat production in the periphery. First, it is unlikely that there was any intercondition difference in temperature gradients within the body because the cooling period was similar in both conditions. Regarding the second mechanism, distal tissue perfusion would have to increase in the meperidine trial to facilitate an increased afterdrop. The lower average Tsk and total heat flux during meperidine trials are consistent with an actual decrease in cutaneous blood flow. Also, peripheral muscular flow would be expected to decrease along with shivering in the meperidine trials. A decrease in both cutaneous and muscle blood flow would actually attenuate the afterdrop in the meperidine trials. It, therefore, appears that the increased afterdrop with meperidine is mainly due to decreased metabolic heat production. Major loss of shivering heat production significantly impairs buffering of heat loss from the core that occurs when shivering heat attenuates the thermal gradients for convective and conductive heat loss to colder peripheral tissues.
In several ways our results during shivering inhibition approximate the conditions of severe hypothermia. Throughout the rewarming period, meperidine reduced metabolism, ventilation, and heart rate. These responses are similar to those seen in severely hypothermic laboratory animals (28) and human patients (2). Although the tissue temperature gradients in the present study would not be as great as in a severely hypothermic patient, they were enough to evoke a greater afterdrop (1.1°C) than previously reported in spontaneously warming mildly hypothermic humans. In the severely hypothermic condition (i.e., Tco < 30°C), shivering would be completely suppressed (2), basal heat production would be only ~60% of normal (based on the Q10 principle), and there would be greater net heat loss than in the present study (27). These factors could potentiate a large afterdrop of a magnitude similar to those previously reported in nonshivering conditions. Cooled anesthetized dogs have been shown to have an afterdrop of up to 3°C (28), and severely hypothermic prisoners of war (Tes <30°C) had afterdrop values of 3-5°C (1). Such a decrease may be imminently life threatening if the temperature of the heart drops below thresholds for cardiac dysfunction (~28°C) or even to levels where spontaneous arrest may occur (<25°C) (2).
Although it would be preferable to experimentally study actual severely hypothermic subjects, ethical considerations contraindicate such a practice. Although the magnitude of cold stress and the responses to cooling are likely less in the present protocol than in an actual severe hypothermic condition, the metabolic and thermal responses are qualitatively similar. Therefore this shivering-inhibition protocol may be useful to compare the efficacy of various rewarming methods without the competing effect of shivering heat production (17). The slight disinhibition of shivering later in the meperidine trial was likely a result of enhanced central thermal drive during the exaggerated afterdrop and/or the diminished effect of meperidine as it was metabolized (i.e., the half-life of meperidine is 3 h) (20). The protocol could be improved by providing supplemental doses of meperidine during the rewarming period, inducing less hypothermia to decrease the central stimulus for shivering, or using other pharmacological agents such as clonidine (7, 25) or nitrous oxide (24) either alone or in combination with meperidine.
In summary, the present protocol is the first to demonstrate that inhibition of shivering potentiates postcooling afterdrop and attenuates rewarming. This protocol provides an opportunity to compare strategies for treatment of nonshivering hypothermia. These studies could provide valuable information regarding treatment of life-threatening severe hypothermia at the rescue site to present the hypothermic victim in the best possible condition for subsequent hospital treatment.
ACKNOWLEDGEMENTS
We thank Ohmeda, Inc., for the use of the pulse oximeter.
FOOTNOTES
Address for reprint requests: G. G. Giesbrecht, Univ. of Manitoba, Faculty of Physical Education and Recreation Studies, 102 Frank Kennedy Bldg., Winnipeg, MB, Canada R3T 2N2 (E-mail: Giesbrec{at}cc.umanitoba.ca).
Received 1 October 1996; accepted in final form 7 July 1997.
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